ArticleOncology letters2022
Origin recognition complex 1 regulates phospholipase Cδ1 to inhibit cell proliferation, migration and epithelial-mesenchymal transition in lung adenocarcinoma.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Origin recognition complex subunit 1 functions as an oncogenic driver and therapeutic target in cancer.Discover oncology · 2025Review
- Pick-up single-cell proteomic analysis for quantifying up to 3000 proteins in a Mammalian cell.Nature communications · 2024Article
- Phospholipase Family Enzymes in Lung Cancer: Looking for Novel Therapeutic Approaches.Cancers · 2023Review
- Stemness genes and miR-1247-3p expression associate with clinicopathological parameters and prognosis in lung adenocarcinoma.PloS one · 2023Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a common pulmonary malignant disease, lung adenocarcinoma exhibits high mortality and morbidity rate. Phospholipase Cδ1 (PLCD1), an enzyme involved in the homeostasis of energy metabolism, is downregulated in lung adenocarcinoma. According to GEPIA, origin recognition complex 1 (ORC1) is a highly expressed gene in lung adenocarcinoma and is negatively associated with PLCD1. To the best of our knowledge, the present study was the first to investigate the role of ORC1 in regulating PLCD1 in lung adenocarcinoma. According to TCGA database, low expression of PLCD1 was correlated with the low overall survival rate of patients suffering from lung adenocarcinoma. The protein and mRNA expression levels of PLCD1 and ORC1 were detected in A549 cells by western blot analysis and reverse transcription-quantitative PCR, respectively. Cell proliferation, invasion and migration were analyzed by MTT, colony formation, Transwell and wound healing assay. Immunofluorescence staining was adopted to estimate the content of Ki67 and western blot was applied for the evaluation of PLCD1, MMP2, MMP9, E-cadherin, N-cadherin, vimentin, Snail and ORC. The binding interaction between ORC1 and PLCD1 was analyzed using chromatin immunoprecipitation and luciferase reporter enzyme gene assays. The results indicated that PLCD1 was lowly expressed in lung adenocarcinoma cells in comparison with that in 16HBE. When PLCD1 was overexpressed in cancer cells, cell proliferation, invasion and migration were significantly inhibited. However, in the presence of both ORC1 and PLCD1 overexpression, the suppressive effects of PLCD1 overexpression alone on cell proliferation, invasion, migration and EMT were attenuated. In conclusion, ORC1 was indicated to inhibit PLCD1, thus regulating the proliferation, migration and EMT processes of lung adenocarcinoma cells, which suggested that ORC1 might be a target for the treatment of lung adenocarcinoma.
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